Changes of plasma tissue factor and tissue factor pathway inhibitor antigen levels and induction of tissue factor expression on the monocytes in coronary artery disease

Citation
Hk. Kim et al., Changes of plasma tissue factor and tissue factor pathway inhibitor antigen levels and induction of tissue factor expression on the monocytes in coronary artery disease, CARDIOLOGY, 93(1-2), 2000, pp. 31-36
Citations number
30
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
CARDIOLOGY
ISSN journal
00086312 → ACNP
Volume
93
Issue
1-2
Year of publication
2000
Pages
31 - 36
Database
ISI
SICI code
0008-6312(2000)93:1-2<31:COPTFA>2.0.ZU;2-9
Abstract
Background: Several studies have shown that thrombosis and inflammation pla y an important role in the pathogenesis of coronary artery disease (CAD). T issue factor (TF) is responsible for the thrombogenicity of the atheroscler otic plaque and plays a key in triggering thrombin generation. The aim of t his study was to assess the levels of TF and tissue factor pathway inhibito r (TFPI) in patients with angiographically documented CAD and also to evalu ate TF induction on monocytes in vitro in the presence of these plasmas fro m patients with CAD. Methods: Plasma antigen levels of soluble TF and TFPI were measured in 65 CAD patients and 22 healthy controls. Surface TF expres sion on monocytes from a healthy donor treated with plasma samples was eval uated by flow cytometry with a direct double-color immunofluorescence techn ique. Results: Significantly elevated levels of both TF and TFPI were found in CAD patients compared with healthy controls (303.6 +/- 134.1 vs. 187.3 +/- 108.7 pg/ml, p < 0.05; 85.2 +/- 48.6 vs. 65.0 +/- 29.0 ng/ml, p < 0.05) . By flow cytometry, monocytes from a healthy donor displayed higher TF ant igen expression when incubated in the presence of CAD plasmas than in contr ol plasmas (34.6 +/- 10.7 vs. 23.2 +/- 10.2%, p < 0.05). Conclusions:The hi gh levels of circulating TF are present in CAD, which were not sufficiently inhibited by the elevated TFPI plasma levels. Although the source of circu lating TF is unclear, TF induction of monocytes by plasma from CAD patients may contribute to the hypercoagulable state. Copyright (C) 2000 S. Karger AG, Basel.